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PubMed1991

Influence of age on the metabolism of plasma low density lipoproteins in healthy males.

The plasma concentration of the atherogenic low density lipoproteins (LDL) increases with age. To clarify the mechanism of this change, we studied the kinetics of autologous 125I-LDL apolipoprotein B (apo B) in 41 normolipidemic, nonobese healthy males. For comparison, they were divided into three age groups: young, 21-39 yr (n = 18), middle-aged, 40-59 yr (n = 11), and old, 60-80 yr (n = 12). The levels of plasma LDL cholesterol and LDL apo B increased from respectively 3.4 +/- 0.1 (SEM) mmol/liter and 86 +/- 2 mg/dl in the young to 4.1 +/- 0.1 mmol/liter and 95 +/- 3 mg/dl in the old (P less than 0.01), and this increase was linked to a progressively decreased (r = -0.38, P less than 0.02) fractional catabolic rate of LDL apo B (0.348 +/- 0.010 pools per day in the young vs. 0.296 +/- 0.009 pools per day in the old, P less than 0.01). The production rate of LDL apo B did not differ significantly between the groups. The reduced fractional catabolic rate of LDL apo B in the old was not associated with a decrease in binding affinity of the LDL particle to its receptor, as judged from its ability to compete for 125I-LDL fibroblast binding. When hepatic LDL receptor expression was stimulated by cholestyramine treatment in six old males, their LDL apo B fractional catabolic rate increased to the levels observed in the young subjects. We conclude that the increase in LDL which normally occurs with age is explained by a reduced capacity for its removal, and hypothesize that this is mediated via a reduced hepatic LDL receptor expression.

Adult↗
PubMed1995

Reproducing abnormal cholesterol biosynthesis as seen in the Smith-Lemli-Opitz syndrome by inhibiting the conversion of 7-dehydrocholesterol to cholesterol in rats.

The Smith-Lemli-Opitz syndrome is a recessive inherited disorder characterized by neurologic developmental defects and dysmorphic features in many organs. Recently, abnormal cholesterol biosynthesis with impaired conversion of 7-dehydrocholesterol to cholesterol has been discovered in homozygotes. To reproduce the biochemical abnormality, BM 15.766, a competitive inhibitor of 7-dehydrocholesterol-delta 7-reductase, the enzyme that catalyzes the conversion of 7-dehydrocholesterol into cholesterol was fed by gavage to rats. After 14 d, plasma cholesterol concentrations declined from 48 mg/dl to 16 mg/dl and 7-dehydro-cholesterol levels rose from trace to 17 mg/dl. Hepatocytes surrounding the central vein developed balloon necrosis. Stimulating cholesterol synthesis with cholestyramine followed by BM 15.766 produced an additional 40% decline (P < 0.05) in plasma cholesterol and 34% increase in 7-dehydrocholesterol levels compared to the inhibitor alone. Adding 2% cholesterol to the diet during the second week of BM 15.766 treatment increased plasma cholesterol threefold and decreased 7-dehydrocholesterol concentrations 55%. Hepatic 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase activity increased 73% with a 3.9-fold rise in mRNA levels but cholesterol 7 alpha-hydroxylase activity decreased slightly though mRNA levels increased 1.4 times with BM 15.766 treatment. These results demonstrate that BM 15.766 is a potent inhibitor of 7-dehydrocholesterol-delta 7-reductase. The model reproduces abnormal cholesterol biosynthesis as seen in the Smith-Lemli-Opitz syndrome and is useful to test different treatment strategies. Stimulating early steps of cholesterol synthesis worsens the biochemical abnormalities while feeding cholesterol inhibits abnormal synthesis, improves the biochemical abnormalities and prevents liver damage.

Abnormalities, Multiple↗
PubMed1990

Management of multiple cholesterol embolization syndrome--a case report.

A sixty-two-year-old man who underwent coronary angiography and received acute thrombolytic and anticoagulant therapy for acute myocardial infarction developed multisystemic injury, including renal insufficiency and cutaneous manifestations. Fundoscopic examination and skin biopsy specimen led to the diagnosis of multiple cholesterol embolization syndrome (MCES). Discontinuation of anticoagulants and administration of hemostatic (carbazochrome, tranexamic acid, reptilase, and vitamin K) and antihyperlipidemic (cholestyramine and probucol) drugs resulted in temporary improvement of cutaneous and renal disorders and extended survival for about one year. Besides severe aortic atherosclerosis, postmortem examination revealed numerous cholesterol emboli to multiple organs. MCES is a rare but serious complication of left heart catheterization and anticoagulant therapy, and the optimal treatment remains to be established. The authors suggest here that the above-mentioned therapy might be effective for management of MCES.

Anticoagulants↗
PubMed1992

Pediatric preventive cardiology: experience in the Tidewater, Virginia area.

The Division of Pediatric Cardiology began a preventive cardiology program in response to the American Academy of Pediatrics (AAP) Nutrition Committee recommendations on pediatric cholesterol screening. This program has consisted of both public and physician educational programs as well as the treatment of individual hyperlipidemic children. A survey of 67 local pediatricians has revealed that they have not followed the AAP directive for a "family history" approach to pediatric cholesterol screening, with most pediatricians screening all their patients for cholesterol abnormalities. Our dietary treatment program for hyperlipidemic children has given good short-term results, lowering mean total cholesterol concentrations by 10% (23 mg/dl) and mean low density lipoprotein cholesterol (LDL) concentrations by 9.3% (16 mg/dl), as well as decreasing the total cholesterol/high density lipoprotein cholesterol (HDL) ratio by 10% (0.6). The additional use of cholestyramine in nine selected patients has effected even greater mean value decreases of 45 mg/dl or 16% (total cholesterol), 44 mg/dl or 19% (LDL), and 1.3 or 19% (total cholesterol/HDL ratio). All these changes are statistically significant (p less than 0.05). These encouraging short-term results hopefully will promote the long-term goal of decreasing the incidence of coronary artery disease, which remains the leading cause of death in our country.

Analysis of Variance↗
PubMed1998

Gastrointestinal complications of chronic granulomatous disease: case report and literature review.

Chronic granulomatous disease (CGD), an inherited disorder of phagocytic leukocyte function, is characterized by recurrent infections with catalase-positive organisms. Gastrointestinal (GI) tract involvement, present in the majority of affected individuals, may be present initially and recurrently, mimics other entities such as inflammatory bowel disease, and causes substantive morbidity and mortality. Disorders of motility, ulceration, obstruction, and infection (e.g., abscesses) occur from the mouth to the anus and stereotypically manifest with vomiting, diarrhea, abdominal pain, weight loss, and fever. Careful physical examination, in concert with appropriate diagnostic studies, is necessary to delineate intraabdominal pathologic processes. Abdominal radiographs, ultrasonography, computerized tomography, and endoscopy are useful ancillary diagnostic procedures. Drainage of accessible abscesses, antimicrobial therapy based on organisms cultured from blood and tissue, and interferon gamma may lead to suppression or eradication of infections and resolution of symptoms. Corticosteroids are useful for gastric outlet obstruction and sulfasalazine and cyclosporine for large bowel disease. Gallbladder dysfunction may be ameliorated, as in our patient, with administration of cholestyramine.

Child, Preschool↗
PubMed2001

Sevelamer hydrochloride (Renagel), a nonabsorbed phosphate-binding polymer, does not interfere with digoxin or warfarin pharmacokinetics.

Sevelamer hydrochloride (Renagel) is a nonabsorbed phosphate-binding polymer marketed for the treatment of hyperphosphatemia in adult patients receiving hemodialysis. Sevelamer also exhibits bile acid-binding properties resulting in LDL cholesterol lowering. Potential drug interactions between digoxin and warfarin and sevelamer were studied. These two drugs were chosen because they are known to bind to the bile acid-binding polymers, cholestyramine and colestipol. Studies were single dose, crossover, with or without six 2.4 g doses of sevelamer. Plasma concentrations were determined using validated analytical methods. The pharmacokinetic profiles of digoxin and warfarin were not altered by the simultaneous and continued administration of sevelamer. Values for the ratio of ln[AUC(0-infinity)], ln[AUC(0-t)], and ln[Cmax] with and without sevelamer were close to 100%, and the 90% confidence intervals for these ratios were within the 80% to 125% range. It was concluded that sevelamer does not interfere with the absorption or excretion of digoxin or warfarin.

Adult↗
PubMed1991

Simvastatin: a review of its pharmacology and clinical use.

Simvastatin, a chemical derivative of lovastatin, is an antihyperlipidemic medication that inhibits hydroxymethylglutaryl coenzyme A reductase. Animal and clinical data suggest simvastatin is twice as potent as lovastatin. It lowers serum cholesterol by inhibiting hepatic synthesis of cholesterol and, more importantly, by increasing the number of low-density lipoprotein (LDL) receptors present on hepatic cellular membranes. Simvastatin, when used at doses of 40 mg/d in patients with heterozygous familial hypercholesterolemia, significantly reduces total cholesterol (greater than 30 percent) and LDL cholesterol (35-45 percent) and tends to reduce triglycerides and raise high-density lipoprotein (HDL) cholesterol. The agent is also effective in patients with polygenic hypercholesterolemia, familial dysbetalipoproteinemia, and nephrotic syndrome. Addition of cholestyramine to simvastatin enhances the LDL cholesterol-lowering effect to approximately 55 percent. Common clinical adverse effects reported with simvastatin use include headaches and gastrointestinal complaints. Transient elevations in serum transaminases and creatine phosphokinase have also been seen. Based on data currently available, the drug's clinical activity and adverse-effect profile are similar to those of lovastatin. Therefore, there is no need for formularies to contain both medications. To choose between the two, one needs to consider the incidence of adverse effects and the daily cost of each product when used at equally effective doses. That information is now now available and, until it is, a clear recommendation cannot be made. Simvastatin, presently marketed in several countries, is investigational in the U.S. but is expected to be available soon.

Adolescent↗
PubMed2006

Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part V: the discovery of the statins and the end of the controversy.

The first four reviews in this series (Steinberg, D. 2004. J. Lipid Res. 45: 1583-1593; Steinberg, D. 2005. J. Lipid Res. 46: 179-190; Steinberg, D. 2005. J. Lipid Res. 46: 2037-2051; Steinberg, D. 2006. J. Lipid Res. 47: 1-14) traced the gradual accumulation of evidence, evidence of several different kinds, supporting the lipid hypothesis. They tracked the history from Anitschkow's 1913 classic work on the cholesterol-fed rabbit model to the breakthrough 1984 Coronary Primary Prevention Trial, the first large, randomized, double-blind primary intervention trial showing that decreasing blood cholesterol (using cholestyramine) significantly reduces coronary heart disease events. At that point, for the first time, decreasing blood cholesterol levels became an official national public health goal. Still, only a small fraction of patients at high risk were getting appropriate cholesterol-lowering treatment, and a number of important clinical questions remained unanswered. This final review in the series traces the early studies that led to the discovery of the statins and briefly reviews the now familiar large-scale clinical trials demonstrating their safety and their remarkable effectiveness in reducing coronary heart disease morbidity and mortality.

Aged↗
PubMed1994

Luminal bile salts and neurotensin release in the isolated vascularly perfused rat jejuno-ileum.

Bile salts in the distal small intestine are strong stimulants of neurotensin (NT) release, but the underlying mechanisms are not known. They were investigated using an isolated vascularly perfused rat jejuno-ileum preparation. Luminal administration of crude ox bile extract (0.25-1.5%, wt/vol) produced a dose-dependent release of NT-like immunoreactivity (NT-LI), with a maximal effect after infusion of 1% bile extract (500% of basal). Pretreatment of the 1% bile extract with the bile salt-sequestering resin cholestyramine (2%, wt/vol) abolished NT-LI release. Taurocholate (TC), the major bile salt in rats, dose dependently increased the release of NT. The maximal secretion of NT-LI was observed after infusion of 20 mM TC (400% of basal). Taurodeoxycholate (20 mM) was as potent as TC in stimulating NT-LI release, but the threshold concentration of taurodeoxycholate for NT-LI secretion was lower than that of TC. Glycocholate and cholate were 2- to 3-fold less potent than TC in releasing NT-LI over the concentration range 5-20 mM. Luminal infusion of oleic acid (sodium salt; 100 mM) increased by 100% the level of NT-LI in the portal effluent, whereas 20 mM oleate had no effect. In contrast, the micellar form of oleic acid (20 and 100 mM) in bile extract (1%) or TC (20 mM) dose dependently reduced the release of NT-LI induced by bile extract or TC alone. Neither intraarterial tetrodotoxin (10(-6) M), EGTA (2 mM), verapamil (5 x 10(-5) M), nor atropine (10(-5) M) had any effect on TC-induced NT-LI release. These results show that the tauro-conjugated forms of cholic and deoxycholic acid are strong stimulants of NT-LI release. The N-cell response is blunted when bile salts are complexed in the lumen by oleic acid. Finally, bile salt-induced NT-LI release is not mediated by intramural nerves and is not dependent on the activation of calcium channels.

Animals↗
PubMed2001

Difference in subcellular distribution between 45- and 37-kDa mevalonate pyrophosphate decarboxylase in rat liver.

We previously reported that the CP diet (a diet containing 5% cholestyramine and 0.1% pravastatin)-induced new species of 37-kDa mevalonate pyrophosphate decarboxylase (MPD) was characteristically and immunologically very similar to the well-known 45-kDa MPD. In the present study, we found a difference in subcellular distribution between 45- and 37-kDa MPD by cell fractionation and immunoblot analysis. The cytosol fraction contained 45- and 37-kDa MPD. Peroxisomal fraction contained a small amount of 45-kDa MPD, but not 37-kDa MPD. Also, 45-kDa MPD in peroxisome is localized in the matrix. From these data, the difference in subcellular distribution between 45- and 37-kDa MPD may be due to differences in the physiological role of cholesterol biosynthesis in rat liver.

Animals↗
PubMed2003

Change in the protein level of mevalonate pyrophosphate decarboxylase in tissues of mouse by pravastatin.

We previously reported that treatment of rats with a diet containing 0.1% pravastatin and 5% cholestyramine markedly increased mevalonate pyrophosphate decarboxylase (MPD) activity in liver crude extracts compared with nontreated rats. In this study, we examined the change in the protein level of MPD in the tissues of mice administered pravastatin. When MPD content in the tissues of nontreated mice was analyzed by quantitative immunoblotting, a single protein band with an apparent molecular weight of 46 kDa was detected in all tissues and the specific protein content of MPD in liver and kidney was markedly higher than that in other tissues. When MPD content in the tissues of pravastatin-treated mice was analyzed by immunoblotting, MPD was markedly increased (9-fold) only in the liver compared with nontreated mice. Next, when MPD activity was measured in the liver between nontreated and pravastatin-treated mice, MPD activity as well as protein levels were markedly increased (11-fold) in the liver of pravastatin-treated mice compared with nontreated mice. These data suggest that a marked induction of MPD in the liver by pravastatin is responsible for the tissue-specific effect of pravastatin.

Animals↗
PubMed1990

Enhanced fecal excretion of bile acids by a new anion-exchange resin possessing a spacer arm in rats.

The effect of a new polystyrene-based, strongly basic, anion-exchange resin possessing an omega-oxobutyl chain as a spacer arm on the fecal bile acid excretion was investigated in rats and compared with that of Dowex 1-X2, chemically equivalent to cholestyramine. The new resin did produce a significant rise in the total fecal bile acid excretion with its ingestion for a period of 4 weeks. Its promoting activity proved to be 2.0- and 1.8-fold more potent than that of Dowex 1-X2 at the 3rd and 4th week, respectively. These results suggest that the introduction of a spacer arm between the polymer backbone and a functional group would lead to an improvement in the in vivo adsorptive efficiency of the resin.

Animals↗
PubMed2005

Efficacy of colestimide coadministered with atorvastatin in japanese patients with heterozygous familial hypercholesterolemia (FH).

BACKGROUND: Colestimide, a 2-methylimidazole-epichlorohydrin polymer, is a new bile-acid-sequestering resin, that is 4-fold as powerful at lowering low-density lipoprotein cholesterol (LDL-C) as the conventional resin (cholestyramine). Moreover, colestimide has excellent patient compliance because it is available in tablet form. METHODS AND RESULTS: The clinical efficacy of colestimide coadministered with atorvastatin on lipid and apolipoprotein concentrations was examined in 15 patients (M/F=10/5, mean+/-SE age=54+/-9 years) with heterozygous familial hypercholesterolemia (FH). After a period of wash-out of any lipid-lowering drugs, atorvastatin (20-40 mg) was administered to patients for at least 8 weeks, and then 3 g of colestimide was administered for a further 8 weeks. Total and LDL-C significantly (<0.0001) decreased by 35% from 361 to 233 mg/dl and 41% from 274 to 161 mg/dl, respectively. Addition of colestimide caused a further significant 12% and 20% reduction, respectively, from the initial values to 205 and 129 mg/dl, respectively. Colestimide was also effective in reducing serum LDL-C concentrations in heterozygous FH patients with hypertriglyceridemia (triglycerides>or=150 mg/dl). CONCLUSIONS: When monotherapy with atorvastatin is insufficient to treat severely hypercholesterolemic patients, such as those with heterozygous FH, colestimide acts to reinforce the action of statins.

Anion Exchange Resins↗
PubMed1994

Interactions between clinically used drugs and oral contraceptives.

Metabolism of contraceptive compounds may be influenced by various drugs. Of clinical importance is induction by barbiturates, by diphenylhydantoin, and especially by rifampicin, of enzymes that are responsible for degradation of estrogens. The major target is the hepatic microsomal estrogen-2-hydroxylase (cytochrome P450 3A4). Another type of interaction of drugs with disposition and effectiveness of estrogens is impairment of their enterohepatic circulation. This may be due to absorption of biliary estrogen conjugates (e.g., by cholestyramine) or to insufficient cleavage of the conjugate by intestinal bacteria, the latter being observed after administration of antibiotics (e.g., ampicillin, neomycin).

Animals↗
PubMed2006

Past, present, and future therapies for Clostridium difficile-associated disease.

OBJECTIVE: To describe and examine the past, present, and potential future treatment options for Clostridium difficile-associated disease (CDAD). DATA SOURCES: A PubMed search, restricted to English-language articles concerning CDAD, was conducted (1965-October 2006) using the key words Clostridium difficile, diarrhea, vancomycin, metronidazole, immunoglobulin, and recurrence. Additional references were located through review of the bibliographies of cited articles and by visiting www.clinicaltrials.gov. STUDY SELECTION AND DATA EXTRACTION: Articles related to the clinical manifestations, diagnosis, and treatment of CDAD, as well as articles addressing current issues related to CDAD, were included. DATA SYNTHESIS: There have been many investigations into CDAD because of the recent increased incidence and morbidity and mortality of the disease. Various studies examining the changing epidemiology and pathogenicity of C. difficile, as well as new therapies for CDAD with agents such as tolevamer and nitazoxanide, are ongoing. In addition, researchers are investigating probiotics and vaccines to evaluate their effectiveness in preventing CDAD and/or preventing recurrences of CDAD. Studies assessing therapies for refractory CDAD are lacking, although case reports have been published citing treatment strategies using vancomycin enemas, intravenous metronidazole, colestipol and cholestyramine, fecal enemas, bowel irrigation, and immunoglobulin. Furthermore, judicious use of antimicrobials, contact precautions, and adequate environmental cleaning are being evaluated in healthcare institutions as methods for controlling and preventing the spread of C. difficile. CONCLUSIONS: Oral metronidazole is the drug of choice for an initial CDAD episode. Oral vancomycin is an option for patients who cannot take or fail treatment with oral metronidazole. Clinical trials are necessary to define the therapy for initial CDAD that is most appropriate and produces lower recurrence rates compared with oral metronidazole or vancomycin treatment. Moreover, appropriate treatment for patients with multiple recurrences of or refractory CDAD needs to be determined. More studies are also needed assessing prevention of recurrences of CDAD.

Clostridioides difficile↗
PubMed1998

Mode of action and adverse effects of lipid lowering drugs.

Serum lipids, cholesterol and triglycerides are incorporated into hydrophilic lipoproteins, which include chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL) and high density lipoproteins (HDL). An elevated level of these lipoproteins, except for HDL, is the basis of all hyperlipidemias. However, only some of the lipoprotein fractions, particularly LDL and remnant particles, are potential risk factors for atherogenesis and subsequent cardiovascular disease. Several classes of pharmacological agents are currently available to increase the breakdown and reduce the synthesis of LDL and remnant factors. These include nicotinic acid and its analogs, fibric acid derivatives (e.g., clofibrate, gemfibrozil, bezafibrate), bile acid resins (e.g., cholestyramine), HMG-CoA reductase inhibitors (e.g., lovastatin, simvastatin, pravastatin) and probucol. Lipid lowering drugs of different classes have a synergistic effect on lipid metabolism and combination therapy is often used. Lipid lowering drugs are prescribed as long-term preventive therapy in apparently asymptomatic people. Several studies indicate that secondary prevention with lipid lowering drugs is cost-effective, particularly in patients with symptomatic coronary artery disease.

Journal Article↗
PubMed2001

Indigenous drugs and atherosclerosis.

Coronary artery disease (CAD) is a major health problem worldwide and its increasing prevalence in younger age groups is of serious concern. Precipitating factors include changes in lifestyles, food fads and stress, as well as the impact of longevity resulting from the control and prevention of communicable diseases. Dietary practices can often lead to increased levels of lipids in blood or trigger an underlying disposition to atherosclerosis. Hence, dietary modification has been an important method for the management of CAD, with the aim of lowering lipid levels. However, long-term trials have shown that this approach reduces cholesterol and triglycerides only moderately. Drug therapy with clofibrate, cholestyramine, etc., has been successful but some disadvantages limit their long-term use. An alternative approach to the treatment of atherosclerosis has been the use of indigenous drugs. This article reviews some of the drugs of the traditional Indian system of medicine, Ayurveda, which have been shown to possess antiatherogenic properties. (c) 2001 Prous Science. All rights reserved.

Journal Article↗